n nnnPathogen/microbe-associated molecular patterns (PAMPs/MAMPs)trigger plant immunity that forms the first line inducible defensesin plants. The regulatory mechanism of MAMP-triggered immunity,however, is poorly understood. Here, we show that Arabidopsisthaliana transcription factors ETHYLENE INSENSITIVE3 (EIN3)and ETHYLENE INSENSITIVE3-LIKE1 (EIL1), previously known tomediate ethylene signaling, also negatively regulate PAMP-triggeredimmunity. Plants lacking EIN3 and EIL1 display enhanced PAMPdefenses and heightened resistance to Pseudomonas syringae bacteria.Conversely, plants overaccumulating EIN3 are compromised inPAMP defenses and exhibit enhanced disease susceptibility toPseudomonas syringae. Microarray analysis revealed that EIN3and EIL1 negatively control PAMP response genes. Further analysesindicated that SALICYLIC ACID INDUCTION DEFICIENT2 (SID2), whichencodes isochorismate synthase required for pathogen-inducedbiosynthesis of salicylic acid (SA), is a key target of EIN3and EIL1. Consistent with this, the ein3-1 eil1-1 double mutantconstitutively accumulates SA in the absence of pathogen attack,and a mutation in SID2 restores normal susceptibility in theein3 eil1 double mutant. EIN3 can specifically bind SID2 promotersequence in vitro and in vivo. Taken together, our data provideevidence that EIN3/EIL1 directly target SID2 to downregulatePAMP defenses.展开▼
机译：ABSTRACTn n
n TOP n <字体颜色= 464c53>抽象 n 介绍 n 结果 n 讨论 n 方法 n 参考文献 n n nnn病原/微生物相关分子模式（PAMP / MAMP） 触发植物免疫力构成植物的第一线诱导防御 。然而，对MAMP触发的免疫的调节机制 知之甚少。在这里，我们显示拟南芥 拟南芥转录因子ETHINSENE INSENSITIVE3（EIN3） 和ETHINSENE INSENSITIVE3-LIKE1（EIL1），以前称为 介导的乙烯信号传导，也负调控PAMP触发的 免疫。缺少EIN3和EIL1的植物表现出增强的PAMP 防御能力，并且增强了对丁香假单胞菌（Sseudomonas syringae）细菌的抗性。相反，过量积累EIN3的植物在 < / SUP> PAMP防御并表现出对假单胞菌丁香的易感性。微阵列分析显示EIN3 和EIL1负控制PAMP反应基因。 进一步分析表明，水杨酸诱导缺陷2（I）SID2（I），它编码病原体诱导的 SUP> SUP> 水杨酸（SA）的生物合成是EIN3 和EIL1的关键目标。与此一致，在没有病原体攻击的情况下， ein3-1 eil1-1 双突变体 组成性地积累SA， 和 SID2 可恢复 ein3 eil1 双重突变体的正常敏感性。 EIN3可以在体内和体外特异性结合 SID2 启动子 序列。综上，我们的数据提供了 证据，即EIN3 / EIL1直接针对 SID2 以下调 PAMP防御。展开▼
School of Agriculture and Biology, Shanghai Jiaotong University, Shanghai 200240, China|National Institute of Biological Sciences, Beijing 102206, China;
National Institute of Biological Sciences, Beijing 102206, China|State Key Laboratory of Plant Genomics and National Plant Gene Research Center, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China;
Department of Plant Pathology, Kansas State University, Manhattan, Kansas 66506;
Michael Smith Laboratories, University of British Columbia, Vancouver, BC V6T 1Z4, Canada;
National Institute of Biological Sciences, Beijing 102206, China;
National Institute of Biological Sciences, Beijing 102206, China|State Key Laboratory of Plant Genomics and National Plant Gene Research Center, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China;
School of Agriculture and Biology, Shanghai Jiaotong University, Shanghai 200240, China;
State Key Laboratory of Plant Genomics and National Plant Gene Research Center, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China;
Department of Plant Pathology, Kansas State University, Manhattan, Kansas 66506;
Michael Smith Laboratories, University of British Columbia, Vancouver, BC V6T 1Z4, Canada;
National Laboratory of Protein Engineering and Plant Genetic Engineering, College of Life Sciences, Peking University, Beijing 100871, China;
National Institute of Biological Sciences, Beijing 102206, China;
